ライフサイエンスコーパス: BPD

1 BPD is now recognized as the result of an aberrant repar

2 BPD is the most common serious complication experienced

3 BPD-diagnosis was ascertained between 1997 and 2013, 11,

4 supplementation (range) was 5.5 days (0-21) (BPD) compared with 2.0 days (0-26) (non-BPD).

5 Median LOS (range) was 7.2 days (4-23) (BPD) compared with 2.5 days (1-30) (non-BPD).

6 ned between 1997 and 2013, 11,665 received a BPD-diagnosis.

7 (benzoporphyrin derivative monoacid ring A; BPD) is increased by the in vivo administration of erlot

8 Adding BPD status at 36 weeks PMA to the model did not change t

9 tes to the decreased serum cholesterol after BPD.

10 sensitivity and cholesterol metabolism after BPD.

11 n obese subjects and reduced to normal after BPD.

12 Seven weeks after BPD, insulin sensitivity had doubled and serum cholester

13 .06), medical NEC (1.57), sepsis (1.43), and BPD (1.30) (P < 0.001).

14 ociation signals for both SCZ (P<10(-7)) and BPD (P=0.029).

15 ne receptor-dependent exacerbation of AA and BPD in mice.

16 ontributing to increased incidence of AA and BPD in the progenies.

17 y SS-exposed mice exhibit exacerbated AA and BPD that is not dependent on the decrease in peroxisome

18 er the observed comorbidity between ADHD and BPD could be due to shared genetic risks.

19 m-based genetic correlation between ADHD and BPD in the full and age-restricted samples (rGfull = .64

20 m-based genetic correlation between ADHD and BPD is substantial, significant, and consistent with the

21 xistence of genetic overlap between ADHD and BPD, with potential differential genetic mechanisms invo

22 isorders of ECM homeostasis such as COPD and BPD, providing a critical mechanism for proteolytic dama

23 p to hospital discharge, including death and BPD at 36 weeks' postmenstrual age.

24 en between pulmonary arterial blood flow and BPD outcomes.

25 of NSAID treatment for PDA on mortality and BPD.

26 miR-34a improves the pulmonary phenotype and BPD-associated pulmonary arterial hypertension (PAH) in

27 he genes differentially expressed in SCZ and BPD are concordant in their expression level (q0.01, 53

28 expression and association for both SCZ and BPD.

29 nates with respiratory distress syndrome and BPD.

30 lling for gestational age, birth weight, and BPD severity, MR-EI was associated with LOS and duration

31 disease, the underlying associations between BPD and ROP are not well characterized.

32 Combined BPD or death rates across 116 NICUs varied from 17.7% to

33 mechanical ventilation and corticosteroids), BPD remains the most frequent complication of extreme pr

34 ression controlled for important covariates, BPD was significantly negatively correlated with lobar a

35 d should be considered when updating current BPD severity definitions.

36 val (95% CI) 0.25-1.55] (P = 0.31) for death/BPD for conventional mechanical ventilation vs high-freq

37 able chromophore (benzoporphyrin derivative, BPD) in the lipid bilayer, and a nanoparticle containing

38 preterm infants who now survive and develop BPD, we hypothesized that risk loci underlying this dise

39 cells of premature infants who later develop BPD or die have impaired mitochondrial bioenergetic capa

40 , HUVECs obtained from infants who developed BPD or died had a lower maximal oxygen consumption rate

41 ypertension increase the odds for developing BPD after preterm birth, and that maternal smoking is st

42 with level IV NICUs, the risk for developing BPD was higher for level II NICUs (odds ratio, 1.23; 95%

43 a well-recognized risk factor for developing BPD.

44 scale family studies of clinically diagnosed BPD are lacking.

45 ion and heritability of clinically diagnosed BPD.

46 Infants with diagnosed BPD had significantly greater volume of high-signal lung

47 zed clinical trials of adults with diagnosed BPD randomized to psychotherapy exclusively or to a cont

48 PD, six premature patients without diagnosed BPD, and six full-term NICU patients (gestational ages,

49 femur length (FL), and biparietal diameter (BPD) during gestation were measured by ultrasounds.

50 agnosis of asthma, reactive airways disease, BPD exacerbation, bronchiolitis, or pneumonia, or a resp

51 by two of the most potent neonatal diseases, BPD and ROP.

52 tivity disorder (ADHD) and bipolar disorder (BPD) are frequently co-occurring and highly heritable me

53 ), schizophrenia (SCZ) and bipolar disorder (BPD) are of great societal and medical importance, but t

54 of schizophrenia (SZ) and bipolar disorder (BPD), and use functional magnetic resonance imaging (fMR

55 our groups: schizophrenia, bipolar disorder (BPD), major depression (MD) and unaffected controls.

56 ciated with borderline personality disorder (BPD) features in the domain of social media.

57 studies of Borderline Personality Disorder (BPD) have found familial aggregation and genetic propens

58 Borderline personality disorder (BPD) is a debilitating condition, but several psychother

59 gression in borderline personality disorder (BPD) is thought to be mediated through emotion dysregula

60 s common in borderline personality disorder (BPD), especially when severe, and the molecular underpin

61 tients with borderline personality disorder (BPD), with impulsivity and emotional dysregulation as co

62 Although borderline personality disorder (BPD)-one of the most common, burdensome, and costly psyc

63 observed in borderline personality disorder (BPD).

64 symptoms of borderline personality disorder (BPD).

65 the BRIDGE Bleeding and Platelet Disorders (BPD) collection who carry a TPM4 variant that causes tru

66 l bypass surgery (biliopancreatic diversion [BPD]).

67 Although the mechanisms driving BPD remain uncertain, exposure to hyperoxia is thought t

68 ve cells pre-loaded with the photoactive dye BPD.

69 igh incidence of bronchopulmonary dysplasia (BPD) and chronic respiratory morbidity.

70 creased risk for bronchopulmonary dysplasia (BPD) and pulmonary hypertension (PH) after preterm birth

71 erm infants with bronchopulmonary dysplasia (BPD) and pulmonary hypertension (PH) have accelerated lu

72 creased risk for bronchopulmonary dysplasia (BPD) and respiratory disease during early childhood afte

73 Bronchopulmonary dysplasia (BPD) and retinopathy of prematurity (ROP) are two debili

74 nt risk factors, bronchopulmonary dysplasia (BPD) and retinopathy of prematurity (ROP), with cortical

75 rate of death or bronchopulmonary dysplasia (BPD) but may cause long-term adverse effects in very pre

76 of infants with bronchopulmonary dysplasia (BPD) demonstrate impaired alveolar development with larg

77 e risk of AA and bronchopulmonary dysplasia (BPD) in children and animal models.

78 pathogenesis of bronchopulmonary dysplasia (BPD) in neonates, for which no specific preventive or th

79 risk factor for bronchopulmonary dysplasia (BPD) in premature infants, a disease characterized by dy

80 Bronchopulmonary dysplasia (BPD) is a chronic disease of preterm babies with poor cl

81 Bronchopulmonary dysplasia (BPD) is a disease prevalent in preterm babies with a nee

82 Rationale: Bronchopulmonary dysplasia (BPD) is a leading complication of preterm birth that aff

83 Bronchopulmonary dysplasia (BPD) is a prevalent yet poorly characterized pulmonary c

84 Bronchopulmonary dysplasia (BPD) is characterized by lifelong obstructive lung disea

85 Bronchopulmonary dysplasia (BPD) occurs in approximately 40% of infants born at youn

86 Bronchopulmonary dysplasia (BPD) remains a major respiratory illness in extremely pr

87 ciated with high bronchopulmonary dysplasia (BPD) risk in preterm infants.

88 a mouse model of bronchopulmonary dysplasia (BPD) that mesenchymal stem cells (MSC) protect against h

89 pathogenesis of bronchopulmonary dysplasia (BPD), a chronic lung disease of prematurity that often l

90 ogenesis akin to bronchopulmonary dysplasia (BPD), a neonatal chronic lung disease.

91 k for developing bronchopulmonary dysplasia (BPD), but its relationship with late respiratory outcome

92 erm infants with bronchopulmonary dysplasia (BPD), but whether early signs of pulmonary vascular dise

93 urity, including bronchopulmonary dysplasia (BPD), cause mortality and morbidity later in life.

94 comes, including bronchopulmonary dysplasia (BPD), in preterm infants.

95 Bronchopulmonary dysplasia (BPD), the main consequence of prematurity, has a signifi

96 e: Patients with bronchopulmonary dysplasia (BPD)-associated pulmonary hypertension (PH) have increas

97 Bronchopulmonary dysplasia (BPD)-associated pulmonary hypertension (PH) is an infant

98 severe forms of bronchopulmonary dysplasia (BPD).

99 5 years old with bronchopulmonary dysplasia (BPD).

100 rders, including bronchopulmonary dysplasia (BPD).

101 birth, including bronchopulmonary dysplasia (BPD).

102 iseases (asthma; bronchopulmonary dysplasia (BPD); and chronic obstructive pulmonary disease (COPD)).

103 y increased with bronchopulmonary dysplasia (BPD; 1.77), whereas total cost increased with surgical N

104 sfunction termed bronchopulmonary dysplasia (BPD; also known as chronic lung disease).

105 ECM remodeling (bronchopulmonary dysplasia [BPD]).

106 ges were used for the first time to evaluate BPD-related brain abnormalities from resting functional

107 In experiment 2, using an experimental BPD-PH model, rat pups exposed to room air or hyperoxia

108 ent currently fulfilling DSM-IV criteria for BPD (cBPD) (n = 23), a patient in remission for 2 years

109 The case definition for BPD varied substantially in the included studies.

110 analyzed to identify early risk factors for BPD and late PH.

111 In conclusion, a new predictive model for BPD severity that incorporates respiratory assessments b

112 l was to validate a new predictive model for BPD severity that incorporates respiratory assessments b

113 th a twofold (P = 0.04) increase in odds for BPD.

114 ilial aggregation and genetic propensity for BPD, but estimates vary widely.

115 o assess the efficacy of psychotherapies for BPD populations.

116 reterm infants were associated with risk for BPD or death before 36 weeks postmenstrual age.

117 ction was associated with increased risk for BPD.

118 implicated, and their interplay in risk for BPD.

119 gression analysis did not suggest a role for BPD clinical state (p(FWE) > .56) or symptom severity (p

120 nd represents a novel therapeutic target for BPD.

121 ription factors has promise as a therapy for BPD in preterm infants.

122 f 210]) and postnatal corticosteroid use for BPD (41.0% [91 of 222] vs 41.5% [95 of 229]) and the mea

123 dules were also built from RNA-seq data from BPD cases or from MD cases but were not preserved when u

124 The meta-analysis between the full BPD sample identified two genome-wide significant (prs70

125 onventional mechanical ventilation died/ had BPD compared with 43 patients (53.8%) in the high-freque

126 apeutic option to prevent or ameliorate HALI/BPD in neonates.

127 Compared with HC, BPD patients showed relatively increased activation of t

128 esults revealed that individuals with higher BPD trait scores reported posting more often on social m

129 t not identical, results were found in human BPD lung samples.

130 hypoalveolarization, which phenocopies human BPD, and Nrf2 deficiency worsens it.

131 We hypothesized that this approach improves BPD risk assessment, particularly in extremely premature

132 In BPD, PFC and ACC MAO-A VT were positively correlated wit

133 hat structural and functional abnormality in BPD involves both temporolimbic and frontomedial structu

134 shold showed a convergence of alterations in BPD patients in genual and perigenual structures, with f

135 sly reported amygdala habituation deficit in BPD and probed this neural phenotype for associations wi

136 d that impairment of alveolar development in BPD results in a decrease in both D(M) and Vc components

137 upport the hypothesis that CC dysfunction in BPD and SZ reflects a continuum of deficits that cuts ac

138 Cross-brain information flow in BPD was examined from May 25, 2012, to December 4, 2015,

139 report on deficient amygdala habituation in BPD and link this neural phenotype to early adversity, a

140 ify with high confidence genes implicated in BPD, thereby providing important insights into its biolo

141 ge more specific studies on RSV infection in BPD patients, including vaccine development and RSV-spec

142 larization and septal thickening observed in BPD.

143 ted pulmonary arterial hypertension (PAH) in BPD mouse models, which, conversely, is worsened by miR-

144 ors, such as neurodevelopmental processes in BPD or adhesion molecules in COPD, are also highlighted.

145 habituation to repeated negative stimuli in BPD (p(FWE) = .015, peak-level familywise error [FWE] co

146 As such, in BPD, a potential role for variants near CRP gene is prop

147 The wide variability in BPD occurrence across hospitals could offer insights int

148 Secondary outcomes included BPD severity, postnatal corticosteroid use, respiratory

149 showed nonsignificant differences, including BPD (55.2% with hydrocortisone vs 50.0% with placebo; ri

150 ltiple indicators of BPD severity, including BPD symptomatology, mood symptoms, suicidality, and neur

151 levels in preterm infants predict increased BPD-PH risk and early Klotho supplementation prevents BP

152 n in a rat model of chorioamnionitis-induced BPD caused by antenatal inflammation.Methods: Endotoxin

153 ecreased and the extent of hyperoxia-induced BPD and PH increased in ADM(+/-) mice compared with ADM(

154 othesized that AM resolves hyperoxia-induced BPD and PH via endothelial nitric oxide synthase (NOS3).

155 netic mechanisms involved in early and later BPD onset.

156 tofrontal cortex coupling were shown in male BPD patients, while in female patients trait anger posit

157 x group interaction was found in which male BPD patients revealed higher activity in the left amygda

158 sulting in alveolar simplification mimicking BPD in neonatal mice, but the underlying mechanisms rema

159 y, in severe BPD subjects (n = 14), moderate BPD subjects (n = 14), subjects with a major depressive

160 tal of 52 infants (31 severe BPD, 9 moderate BPD, and 12 with either mild or no BPD) were imaged betw

161 PFC and ACC MAO-A VT compared with moderate BPD, MDE, and healthy control subjects (multivariate ana

162 After irradiation at 690 nm, BPD disrupted the endosomal membranes and delivered the

163 moderate BPD, and 12 with either mild or no BPD) were imaged between 39 and 47 weeks postmenstrual a

164 21) (BPD) compared with 2.0 days (0-26) (non-BPD).

165 23) (BPD) compared with 2.5 days (1-30) (non-BPD).

166 >6 days) in those with BPD compared with non-BPD (OR, 11.9; 95% CI, 1.4-100; P = .02).

167 er among children with BPD compared with non-BPD: RSV hospitalization (odds ratio [OR], 2.6; 95% conf

168 en with BPD compared with those without (non-BPD).

169 imaging and phenotypical characterization of BPD severity levels.

170 are consistent with the conceptualization of BPD as an emotion dysregulation disorder.

171 n addition, at least some neural deficits of BPD may be more reversible than is currently assumed for

172 ssociated with the subsequent development of BPD or PH at 36 weeks post-menstrual age (PMA) is unknow

173 ome is a key mechanism in the development of BPD, and represents a novel therapeutic target for BPD.

174 ls with unknown impact on the development of BPD.

175 masome is associated with the development of BPD.

176 Of the 14396 individuals with a diagnosis of BPD, 6671 were included in the cohort, with 2148 prescri

177 e investigated the early and late effects of BPD on plasma BA levels, composition, and markers of BA

178 f erlotinib; nevertheless, this elevation of BPD levels only partially accounts for the benefit of er

179 were simultaneously examined for evidence of BPD-like lung injury, investigating both the short- and

180 s11265269 was identified as a risk factor of BPD (OR 1.8, p = 5.3 x 10(-5)), independently of the rob

181 mbic brain regions are a hallmark feature of BPD and therefore are consistent with the conceptualizat

182 or a core diagnostic and clinical feature of BPD.

183 VT is associated with multiple indicators of BPD severity, including BPD symptomatology, mood symptom

184 Using a neonatal mouse model of BPD, we show that hyperoxia increases activity and expre

185 stantially up-regulated in a murine model of BPD.

186 h and prevents PH in two antenatal models of BPD induced by intraamniotic exposure to endotoxin (ETX)

187 ation of mechanical ventilation, the odds of BPD were only increased among infants exposed to 4 or mo

188 nfants, or 44.8%, met the primary outcome of BPD or death prior to 36 weeks.

189 Greater insights into the pathobiology of BPD will provide a better understanding of disease mecha

190 ly PVD may contribute to the pathobiology of BPD.

191 ovide a novel strategy for the prevention of BPD in preterm infants.

192 ar adjusted hazard ratios, i.e., the rate of BPD-diagnoses in relatives to individuals with BPD-diagn

193 Rates of BPD have not improved over the past two decades; nor hav

194 d plasma levels of CRP predicted the risk of BPD (OR 3.4, p = 2.9 x 10(-4)) and the SNP rs3093059 ass

195 from the first week of life and the risk of BPD were assessed.

196 al therapeutic strategy for the treatment of BPD.

197 itors can be beneficial for the treatment of BPD.

198 To further elucidate neural underpinnings of BPD, the present meta-analysis summarizes functional neu

199 ientific evidence to guide future updates of BPD severity definitions.

200 uals with BPD (5167 thereof with early-onset BPD), and 21,363 typically developing controls.

201 ng characteristic analysis to define optimal BPD severity levels using the duration of supplementary

202 ratio, 0.73; 95% CI, 0.43-1.13; P = .18), or BPD (odds ratio, 1.01; 95% CI, 0.73-1.45; P = .94) in su

203 red to controls, preterm infants with BPD or BPD-PH had decreased cord Klotho levels.

204 primary outcome was a composite of death or BPD assessed at 36 weeks' postmenstrual age.

205 ot improve the composite outcome of death or BPD at 36 weeks' postmenstrual age.

206 tnatal CMV on the combined risk for death or BPD at 36 weeks' postmenstrual age.

207 Death or BPD occurred in 128 of 181 infants (70.7%) randomized to

208 NSAID treatment and the odds of mortality or BPD (odds ratio, 0.94; 95% CI, 0.70-1.25; P = .69), mort

209 ence in the combined outcome of mortality or BPD between the 2 ventilation groups in prenatally diagn

210 and prevented RVH in antenatal and postnatal BPD models.

211 nts, but whether IGF-1 treatment can prevent BPD or PH is unknown.Objectives: To evaluate whether pos

212 rapy may provide novel strategies to prevent BPD due to antenatal inflammation.

213 losure in improving mortality and preventing BPD is unclear.

214 sk and early Klotho supplementation prevents BPD-like phenotype and PH in rodents exposed to neonatal

215 ased regionalization of NICU care may reduce BPD among VLBW infants.

216 proves lung structure and function in rodent BPD models, severe side effects of VEGF therapy prevent

217 Overall, our study is the first to sequence BPD exomes from newborn blood spot samples and identify

218 Severe BPD was associated with greater PFC and ACC MAO-A VT com

219 PD.Methods: A total of 52 infants (31 severe BPD, 9 moderate BPD, and 12 with either mild or no BPD)

220 d to recapitulate mild, moderate, and severe BPD, using two different strains of mice, in males and f

221 Rates for severe BPD (26.6% [55 of 207] vs 20.5% [43 of 210]) and postnat

222 ls in PFC and ACC would be highest in severe BPD and would correlate with symptom magnitude.

223 -A VT), an index of MAO-A density, in severe BPD subjects (n = 14), moderate BPD subjects (n = 14), s

224 in the odds of mortality or moderate/severe BPD among similar preterm infants born at 28 weeks or yo

225 DA in reducing mortality and moderate/severe BPD at 36 weeks postmenstrual age.

226 lification, only appeared in the most severe BPD cases, although cystic appearance did increase with

227 e, and the molecular underpinnings of severe BPD are largely unknown.

228 osite outcome was death, moderate, or severe BPD at 36 weeks postmenstrual age.

229 In the severe BPD mouse model, administering miR-146 mimic to males at

230 is an urgent need to establish standardized BPD case definitions, review the RSV prophylaxis guideli

231 We hypothesized that BPD cases with an early age of onset (</=21 years old) w

232 Inhibition of Wnt5A abrogated the BPD transcriptomic phenotype induced by hyperoxia.

233 targets of miR34a, is able to ameliorate the BPD pulmonary and PAH phenotypes.

234 e D(M)/Vc ratio would not differ between the BPD and FT groups.

235 In the BPD mouse model, gonadotropin-releasing hormone was incr

236 recombinant Wnt5a reproduced features of the BPD phenotype in PCLS cultured in normoxic conditions.

237 ese findings suggest that in addition to the BPD diagnosis at 36 weeks, other factors modulate late r

238 and morphogenesis and may contribute to the BPD phenotype when impaired.

239 nt social media use, and then assessed their BPD features using the short form of the Five-Factor Bor

240 diction of respiratory outcomes according to BPD severity.

241 Restricting the analyses to BPD cases with an early onset yielded one genome-wide si

242 t perinatal Klotho deficiency contributes to BPD-PH risk and strategies that preserve Klotho levels,

243 o identify gene loci predisposing infants to BPD.

244 The biological mechanisms leading to BPD are not fully understood, although an arrest in lung

245 dies have shown that males are more prone to BPD and have a delayed recovery compared with females, f

246 for the discovery of novel targets to treat BPD and ROP.

247 er revealed a continuum of deficits in which BPD showed intermediate levels of CC relative to control

248 f interpersonal difficulties associated with BPD features even in the non-clinical population, and de

249 e interpersonal difficulties associated with BPD features, and to inform and assess therapeutic inter

250 leotide polymorphisms (SNPs) associated with BPD were genotyped in both Finnish (n = 555) and non-Fin

251 d birth weight z-scores were associated with BPD.

252 ically significant inverse associations with BPD, HC, and BW when using maternal serum, and for AC an

253 ing rs3093059, had nominal associations with BPD.

254 Risks were higher among children with BPD compared with non-BPD: RSV hospitalization (odds rat

255 tal case fatality (hCFR) among children with BPD compared with those without (non-BPD).

256 e is considerably higher among children with BPD.

257 MRI and echo indices were compared with BPD severity and clinical outcomes, including length of

258 resonance imaging (MRI) will correlate with BPD severity and predict short-term clinical outcomes, i

259 Twenty-two percent of infants diagnosed with BPD and 34% of preterm infants without BPD had no clinic

260 Length of stay increased with BPD (2.92) and NEC (surgical, 2.04; medical, 1.28) (P <

261 and Main Results: PA/AO ratio increased with BPD severity.

262 individuals with ADHD, 9650 individuals with BPD (5167 thereof with early-onset BPD), and 21,363 typi

263 D-diagnoses in relatives to individuals with BPD-diagnosis compared to individuals with unaffected re

264 increased the odds of having an infant with BPD by twofold (P = 0.02).

265 y length and did not differ for infants with BPD and FT subjects.

266 ncreasing body length; however, infants with BPD had significantly lower D(M) and Vc than FT subjects

267 ur findings are consistent with infants with BPD having impaired alveolar development with fewer but

268 s compared to controls, preterm infants with BPD or BPD-PH had decreased cord Klotho levels.

269 whether the decreased DL(CO) in infants with BPD results from a reduction in both components of DL(CO

270 T was decreased in the lungs of infants with BPD.

271 thology similar to that seen in infants with BPD.

272 uding need for PH therapies for infants with BPD.Methods: A total of 52 infants (31 severe BPD, 9 mod

273 In the aggression phase, men with BPD exhibited higher activity in the lateral orbitofront

274 erity and clinical outcomes in neonates with BPD.

275 We examined a sample of 120 patients with BPD and 115 healthy control subjects with a well-establi

276 ay matter abnormalities in 263 patients with BPD and 278 HC were analyzed.

277 tral stimuli in a total of 281 patients with BPD and 293 healthy control subjects (HC) were included.

278 hirty-three female and 23 male patients with BPD and 30 healthy women and 26 healthy men participated

279 imaging data were acquired in patients with BPD and in an equal number of matched control subjects (

280 adjustment of behavior in male patients with BPD despite their efforts at control.

281 the respiratory problems that patients with BPD experience.

282 aggression in female and male patients with BPD have been widely missing on the behavioral and parti

283 ntrols, 24 recent (<1 y) onset patients with BPD Type I with psychotic features, and 70 recent onset

284 ignificant differences between patients with BPD, premature patients without BPD, and full-term contr

285 during quiet breathing in six patients with BPD, six premature patients without diagnosed BPD, and s

286 connectivity was found in male patients with BPD.

287 ioral and clinical symptoms in patients with BPD.

288 are nonsynonymous mutations in patients with BPD.

289 EGF therapy prevent its use in patients with BPD.Objectives: To test whether nanoparticle delivery of

290 e interaction difficulties among people with BPD.

291 as more often longer (>6 days) in those with BPD compared with non-BPD (OR, 11.9; 95% CI, 1.4-100; P

292 noxide (DL(CO)) in infants and toddlers with BPD compared with healthy controls born at full term (FT

293 2%; P = 0.020) and premature infants without BPD (8.2 +/- 6.4%; P = 0.026).

294 with BPD and 34% of preterm infants without BPD had no clinical signs of late respiratory disease du

295 atients with BPD, premature patients without BPD, and full-term control subjects.

296 be safe but did not improve survival without BPD at 36 weeks' PMA or respiratory and neurodevelopment

297 Survival without BPD at 36 weeks' PMA was similar between the placebo and

298 ary outcome was the rate of survival without BPD at 36 weeks' postmenstrual age (PMA).

299 to 14 improves the rate of survival without BPD.

300 ith HUVECs from infants who survived without BPD, HUVECs obtained from infants who developed BPD or d